Experimental models of mitochondrial diseases typically involve inhibition of enzymes involved in the electron transport chain (1). It has been further reported that many neurodegenerative diseases are associated with mitochondrial dysfunction (2-5). Defects in complexes I, II and IV of the mitochondrial respiratory chain have been detected in Alzheimer's, Parkinson's, Huntington's and Lou Gehrig's diseases (6-9).
Several lines of evidence implicate that Parkinson's Disease (PD) is a free radical disease involving mitochondrial dysfunction leading to failure of energy production (10-11). Increased oxidative damage, dopamine depletion, protein nitration, iron accumulation, protein aggregation, and apoptosis are characteristic hallmarks of Parkinson's Disease (12-14).
Numerous antioxidants and iron chelators have been utilized in Parkinson's Disease animal models and patients with little or limited success (15-16). Apocynin is a naturally occurring methoxy-substituted catechol that has been shown to inhibit NADPH-oxidase (17). Apocynin has the structure depicted below:

Apocynin has also been reported to form a dimer by peroxidase oxidation (17), such as depicted below:

While the usefulness of various apocynin derivatives has been reported in the literature (2-5), their potential as therapeutic drugs in neurodegenerative diseases, such as Parkinson's disease, has not been established.